<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet type="text/xsl" href="https://www.nitrc.org/themes/nitrc3.0/css/rss.xsl.php?feed=https://www.nitrc.org/export/rss20_forum.php?forum_id=6450" ?>
<?xml-stylesheet type="text/css" href="https://www.nitrc.org/themes/nitrc3.0/css/rss.css" ?>
<rss version="2.0"> <channel>
  <title>NITRC News Group Forum: ketamine-modulates-hippocampal-neurochemistry-and-functional-connectivity--a-combined-magnetic-resonance-spectroscopy-and-resting-state-fmri-study-in-healthy-volunteers.</title>
  <link>http://www.nitrc.org/forum/forum.php?forum_id=6450</link>
  <description>
	&lt;table border=&quot;0&quot; width=&quot;100%&quot;&gt;&lt;tr&gt;&lt;td align=&quot;left&quot;/&gt;&lt;td align=&quot;right&quot;&gt;&lt;a href=&quot;http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&amp;amp;cmd=Link&amp;amp;LinkName=pubmed_pubmed&amp;amp;from_uid=27480494&quot;&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Ketamine modulates hippocampal neurochemistry and functional connectivity: a combined magnetic resonance spectroscopy and resting-state fMRI study in healthy volunteers.&lt;/b&gt;&lt;/p&gt;          
        &lt;p&gt;Mol Psychiatry. 2016 Aug 2;&lt;/p&gt;
        &lt;p&gt;Authors:  Kraguljac NV, Frölich MA, Tran S, White DM, Nichols N, Barton-McArdle A, Reid MA, Bolding MS, Lahti AC&lt;/p&gt;
        &lt;p&gt;Abstract&lt;br/&gt;
        A growing body of evidence suggests glutamate excess in schizophrenia and that N-methyl-d-aspartate receptor (NMDAR) hypofunction on γ-aminobutyric acid (GABA) interneurons disinhibiting pyramidal cells may be relevant to this hyperglutamatergic state. To better understand how NMDAR hypofunction affects the brain, we used magnetic resonance spectroscopy and resting-state functional magnetic resonance imaging (MRI) to study the effects of ketamine on hippocampal neurometabolite levels and functional connectivity in 15 healthy human subjects. We observed a ketamine-induced increase in hippocampal Glx (glutamate+glutamine; F=3.76; P=0.04), a decrease in fronto-temporal (t=4.92, PFDR&amp;lt;0.05, kE=2198, x=-30, y=52, z=14) and temporo-parietal functional connectivity (t=5.07, PFDR&amp;lt;0.05, kE=6094, x=-28, y=-36, z=-2), and a possible link between connectivity changes and elevated Glx. Our data empirically support that hippocampal glutamatergic elevation and resting-state network alterations may arise from NMDAR hypofunction and establish a proof of principle whereby experimental modelling of a disorder can help mechanistically integrate distinct neuroimaging abnormalities in schizophrenia.Molecular Psychiatry advance online publication, 2 August 2016; doi:10.1038/mp.2016.122.&lt;br/&gt;
        &lt;/p&gt;&lt;p&gt;PMID: 27480494 [PubMed - as supplied by publisher]&lt;/p&gt;
    </description>
  <language>en-us</language>
  <copyright>Copyright 2000-2026 NITRC OSI</copyright>
  <webMaster></webMaster>
  <lastBuildDate>Tue, 05 May 2026 1:16:52 GMT</lastBuildDate>
  <docs>http://blogs.law.harvard.edu/tech/rss</docs>
  <generator>NITRC RSS generator</generator>
 </channel>
</rss>
